Difference between revisions of "Team:TP-CC San Diego"

 
(483 intermediate revisions by 3 users not shown)
Line 1: Line 1:
−
{{:Team:TP-CC_San_Diego/Templates/Header}}
 
 
{{:Team:TP-CC_San_Diego/Templates/NavBar}}
 
{{:Team:TP-CC_San_Diego/Templates/NavBar}}
−
{{:Team:TP-CC_San_Diego/Templates/CSS}}
+
{{:Team:TP-CC San Diego/Templates/Font}}
−
 
+
{{:Team:TP-CC_San_Diego/Templates/AnimationCSS}}
  
 
<html>
 
<html>
 
<head>
 
<head>
 +
<title>Home</title>
 +
 +
<link href="https://cdn.rawgit.com/michalsnik/aos/2.1.1/dist/aos.css" rel="stylesheet">
 +
<script src="https://cdn.rawgit.com/michalsnik/aos/2.1.1/dist/aos.js"></script>
 +
<script>
 +
    AOS.init();
 +
</script>
 +
 
<style>
 
<style>
  
−
div.sub-content
+
.main-title {
 +
  padding: 40px 80px 40px 80px;
 +
  font-size: 50px;
 +
  padding-top: 6%;
 +
}
 +
 
 +
.fade-in{
 +
  animation: opac 2s
 +
}
 +
@keyframes opac{
 +
from{opacity:0}
 +
to{opacity:1}}
 +
 
 +
.icon-wrapper
 
{
 
{
−
   height: 100%
+
   display: inline-block;
−
   width: 60%;
+
   margin: 1%;
 
}
 
}
  
−
</style>
+
.icon
 +
{
 +
  width:  100%;
 +
  height: 100%;
 +
  margin: 0 auto auto auto;
 +
}
  
 +
.icon img
 +
{
 +
  position: block;
 +
  width: 100%;
 +
  height: 100%;
 +
}
 +
 +
.icon-wrapper h3
 +
{
 +
  position: relative;
 +
  margin: auto;
 +
  top: -15%;
 +
  text-align: center;
 +
}
 +
 +
.imageDiv
 +
{
 +
    display: inline-block;
 +
 +
}
 +
 +
.info
 +
{
 +
  margin: 2% auto auto auto;
 +
  font-size: 20px;
 +
  font-family: 'Poppins', sans-serif;
 +
  color: black;
 +
  text-align: center;
 +
}
 +
 +
.banner
 +
{
 +
  padding-top: -1%;
 +
}
 +
 +
.text-wrapper1
 +
{
 +
    background: none;
 +
    margin: 80px 0px 0px 2%;
 +
    padding: 2% 2% 2% 2%;
 +
    width: 80%;
 +
    height: 100%;
 +
    margin: auto;
 +
 +
}
 +
</style>
 
</head>
 
</head>
 +
<body>
 +
 +
<center>
 +
<div class="banner">
 +
<img style="width: 100%;margin: auto auto .5% auto;" src="https://static.igem.org/mediawiki/2017/archive/1/11/20171029225547%21T--TP-CC_San_Diego--banner.png">
 +
</div>
 +
</center>
 +
<!--<center>
 +
<h2 class = "main-title fade-in" style="margin: 5% 0 5% 0;">ecDNA</h2>
 +
-->
 +
 +
 +
<div class="text-wrapper1">
 +
  <h3 class="day" style="margin-top: 2%;">Abstract</h3>
 +
<p style="font-size: 22px; margin-top: 20px;">
 +
Cancer, a genetic disease resulting in uncontrollable cell growth, is mostly caused by somatic mutations acquired throughout an individual’s lifetime. Because it induces the increased expression of growth related genes, oncogene amplification is one of the driving forces of cancer cell replication. Recently, it was discovered that some oncogenes resided on extrachromosomal DNA (ecDNA). Like the DNA on chromosomes, ecDNAs are double stranded. A key difference, however, is the circular shape of ecDNAs; they are able to randomly distribute because they do not have centromeres, which increases heterogeneity in daughter cells. This can cause the cancerous tumors to develop faster resistance to current treatments. To target the ecDNA, we used CRISPR technology to create double strand breaks specifically in the ecDNA. Because ecDNA causes oncogene copy number to increase exponentially, utilizing CRISPR to create breaks in ecDNA decreases cancer cells’ replication speed.
 +
 +
</p>
 +
</div>
 +
 +
<center>
 +
<div style="margin-top: 2%;">
 +
<div class="icon-wrapper ih-item circle effect10 top_to_bottom"><a href="https://2017.igem.org/Team:TP-CC_San_Diego/Description">
 +
        <div class="icon-wrapper img"><img src="https://static.igem.org/mediawiki/2017/archive/e/e4/20171023064510%21T--TP-CC_San_Diego--brain.png" width = "250"></div>
 +
        <div class="info">
 +
        <h3 class = "page-title">Project Description</h3>
 +
        </div></a>
 +
</div>
 +
 +
<div class="icon-wrapper ih-item circle effect10 top_to_bottom"><a href="https://2017.igem.org/Team:TP-CC_San_Diego/Results">
 +
        <div class="icon-wrapper img"><img src="https://static.igem.org/mediawiki/2017/archive/e/e1/20171023064527%21T--TP-CC_San_Diego--beaker.png" width = "250"></div>
 +
        <div class="info">
 +
      <h3 class = "page-title">Results</h3>
 +
        </div></a>
 +
</div>
 +
 +
<div class="icon-wrapper ih-item circle effect10 top_to_bottom"><a href="https://2017.igem.org/Team:TP-CC_San_Diego/Model">
 +
        <div class="icon-wrapper img"><img src="https://static.igem.org/mediawiki/2017/archive/6/6a/20171023064653%21T--TP-CC_San_Diego--graph.png" width = "250"></div>
 +
        <div class="info">
 +
      <h3 class = "page-title">Modeling</h3>
 +
        </div></a>
 +
</div>
 +
</div>
 +
</center>
 +
   
 +
<center>
 +
<div class="icon-wrapper ih-item circle effect10 top_to_bottom"><a href="https://2017.igem.org/Team:TP-CC_San_Diego/LabBook">
 +
        <div class="icon-wrapper img"><img src="https://static.igem.org/mediawiki/2017/archive/d/d7/20171023064353%21T--TP-CC_San_Diego--book.png" width = "250"></div>
 +
        <div class="info">
 +
      <h3 class = "page-title">Lab Notebook</h3>
 +
        </div></a>
 +
</div>
  
−
<body style="padding-top: 200px;">
+
<div class="icon-wrapper ih-item circle effect10 top_to_bottom"><a href="https://2017.igem.org/Team:TP-CC_San_Diego/InterLab">
−
<h2 class = "main-title">ecDNA</h2>
+
        <div class="icon-wrapper img"><img src="https://static.igem.org/mediawiki/2017/archive/2/2d/20171023064557%21T--TP-CC_San_Diego--cell.png" width = "250"></div>
 +
        <div class="info">
 +
      <h3 class = "page-title">Interlab Study</h3>
 +
        </div></a>
 +
</div>
 +
<div class="icon-wrapper ih-item circle effect10 top_to_bottom"><a href="https://2017.igem.org/Team:TP-CC_San_Diego/Protocols">
 +
        <div class="icon-wrapper img"><img src="https://static.igem.org/mediawiki/2017/archive/0/03/20171023064720%21T--TP-CC_San_Diego--magnifying.png" width = "250"></div>
 +
        <div class="info">
 +
      <h3 class = "page-title">Protocols</h3>
 +
        </div></a>
 +
</div>
 +
</center>
 +
   
 +
<center>
 +
<div class="icon-wrapper ih-item circle effect10 top_to_bottom"><a href="https://2017.igem.org/Team:TP-CC_San_Diego/MedalCriteria">
 +
        <div class="icon-wrapper img"><img src="https://static.igem.org/mediawiki/2017/archive/4/4a/20171023064737%21T--TP-CC_San_Diego--medal.png" width = "250"></div>
 +
        <div class="info">
 +
      <h3 class = "page-title">Medal Criteria</h3>
 +
        </div></a>
 +
</div>
  
−
<p> Cancer, a genetic disease resulting in uncontrollable cell growth, is mostly caused by somatic mutations acquired throughout an individual’s lifetime. Because it induces the increased expression of growth related genes, oncogene amplification is one of the driving forces of cancer cell replication. Recently, it was discovered that some oncogenes resided on extrachromosomal DNA (ecDNA). Like the DNA on chromosomes, ecDNAs are double stranded. A key difference, however, is the circular shape of ecDNAs; they are able to randomly distribute because they do not have centromeres, which increases heterogeneity in daughter cells. This can cause the cancerous tumors to develop faster resistance to current treatments. To target the ecDNA, we used CRISPR technology to create double strand breaks specifically in the ecDNA. Because ecDNA causes oncogene copy number to increase exponentially, utilizing CRISPR to create breaks in ecDNA decreases cancer cells’ replication speed.</p>
+
<div class="icon-wrapper ih-item circle effect10 top_to_bottom"><a href="https://2017.igem.org/Team:TP-CC_San_Diego/HumanPractices">
 +
        <div class="icon-wrapper img"><img src="https://static.igem.org/mediawiki/2017/archive/e/e7/20171023064751%21T--TP-CC_San_Diego--podium.png" width = "250"></div>
 +
        <div class="info">
 +
      <h3 class = "page-title">Human Practices</h3>
 +
        </div></a>
 +
</div>
  
 +
<div class="icon-wrapper ih-item circle effect10 top_to_bottom"><a href="https://2017.igem.org/Team:TP-CC_San_Diego/Team">
 +
        <div class="icon-wrapper img"><img src="https://static.igem.org/mediawiki/2017/archive/e/e7/20171023064541%21T--TP-CC_San_Diego--ecdnagroup.png" width = "250"></div>
 +
        <div class="info">
 +
      <h3 class = "page-title">Team</h3>
 +
        </div></a>
 +
</div>
 +
</center>
 
</body>
 
</body>
 
</html>
 
</html>

Latest revision as of 00:04, 2 November 2017

Home

Abstract

Cancer, a genetic disease resulting in uncontrollable cell growth, is mostly caused by somatic mutations acquired throughout an individual’s lifetime. Because it induces the increased expression of growth related genes, oncogene amplification is one of the driving forces of cancer cell replication. Recently, it was discovered that some oncogenes resided on extrachromosomal DNA (ecDNA). Like the DNA on chromosomes, ecDNAs are double stranded. A key difference, however, is the circular shape of ecDNAs; they are able to randomly distribute because they do not have centromeres, which increases heterogeneity in daughter cells. This can cause the cancerous tumors to develop faster resistance to current treatments. To target the ecDNA, we used CRISPR technology to create double strand breaks specifically in the ecDNA. Because ecDNA causes oncogene copy number to increase exponentially, utilizing CRISPR to create breaks in ecDNA decreases cancer cells’ replication speed.

Lab Notebook

Interlab Study

Protocols

Medal Criteria

Human Practices

Team